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• W1996740963 abstract "Glucocorticoids promote thymocyte apoptosis and modulate transcription of several genes including GILZ, which is strongly up-regulated in the thymus. We used transgenic mice overexpressing GILZ in the T-cell lineage to investigate TCR-triggered functions of GILZ-overexpressing thymocytes. TCR-triggered apoptosis, but not glucocorticoid-induced apoptosis, was inhibited in transgenic mice compared to their controls. In vivo anti-CD3 administration did not reduce CD4+CD8+ thymocyte number. Analysis of TCR-triggered molecular changes indicated that p65 NF-κB nuclear translocation and DNA binding activity was inhibited in transgenic mice, which might be linked with apoptosis inhibition. IL-10 release increased whereas release of IL-2, IFN-γ, IL-13 and IL-4 remained unchanged. These results support the hypothesis that GILZ regulates, at least in part, T-cell development by influencing thymus function at cellular and molecular levels." @default.
• W1996740963 created "2016-06-24" @default.
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• W1996740963 date "2006-07-01" @default.
• W1996740963 modified "2023-09-28" @default.
• W1996740963 title "Inhibited cell death, NF-κB activity and increased IL-10 in TCR-triggered thymocytes of transgenic mice overexpressing the glucocorticoid-induced protein GILZ" @default.
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• W1996740963 doi "https://doi.org/10.1016/j.intimp.2006.02.001" @default.
• W1996740963 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16714216" @default.
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